nach oben

Journal of Nephrology

Erschienen in:

17.02.2023 | Review

Mitochondrial quality control in acute kidney disease

verfasst von: Jingyi Sheng, Xian Li, Juan Lei, WeiHua Gan, Jiayu Song

Erschienen in: Journal of Nephrology | Ausgabe 5/2023

Einloggen, um Zugang zu erhalten

Abstract

Acute kidney disease (AKD) involves multiple pathogenic mechanisms, including maladaptive repair of renal cells that are rich in mitochondria. Maintenance of mitochondrial homeostasis and quality control is crucial for normal kidney function. Mitochondrial quality control serves to maintain mitochondrial function under various conditions, including mitochondrial bioenergetics, mitochondrial biogenesis, mitochondrial dynamics (fusion and fission) and mitophagy. To date, increasing evidence indicates that mitochondrial quality control is disrupted when acute kidney disease develops. This review describes the mechanisms of mitochondria quality control in acute kidney disease, aiming to provide clues to help design new clinical treatments.

Kellum JA et al (2012) Kidney disease: improving global outcomes (KDIGO) acute kidney injury work group. Kdigo clinical practice guideline for acute kidney injury. Kidney Int Suppl 2:1–138. https://doi.org/10.1038/kisup.2012.1CrossRef

Levin A et al (2013) Kidney Disease: Improving Global Outcomes (KDIGO). Kdigo 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl 3(1):1–150. https://doi.org/10.1038/kisup.2012.73CrossRef

Levey AS (2021) Defining AKD: the spectrum of AKI, AKD, and CKD. Nephron. https://doi.org/10.1159/000516647CrossRefPubMed

Funk JA, Schnellmann RG (2012) Persistent disruption of mitochondrial homeostasis after acute kidney injury. Am J Physiol Ren Physiol 302(7):F853–F864. https://doi.org/10.1152/ajprenal.00035.2011CrossRef

Aparicio-Trejo OE et al (2020) Chronic impairment of mitochondrial bioenergetics and β-oxidation promotes experimental AKI-to-CKD transition induced by folic acid. Free Rad Biol Med 154:18–32. https://doi.org/10.1016/j.freeradbiomed.2020.04.016CrossRefPubMed

Duann P, Lin PH (2017) Mitochondria damage and kidney disease. Adv Exp Med Biol 982:529–551. https://doi.org/10.1007/978-3-319-55330-6_27CrossRefPubMedPubMedCentral

Bhargava P, Schnellmann RG (2017) Mitochondrial energetics in the kidney. Nat Rev Nephrol 13(10):629–646. https://doi.org/10.1038/nrneph.2017.107CrossRefPubMedPubMedCentral

Chawla LS et al (2017) Acute kidney disease and renal recovery: consensus report of the acute disease quality initiative (ADQI) 16 Workgroup. Nat Rev Nephrol. 13(4):241–257. https://doi.org/10.1038/nrneph.2017.2CrossRefPubMed

Levey AS et al (2020) Nomenclature for kidney function and disease: report of a kidney disease: improving global outcomes (KDIGO) consensus conference. Kidney Int. 97(6):1117–1129. https://doi.org/10.1016/j.kint.2020.02.010CrossRefPubMed

10.

Ronco C, Bellomo R, Kellum JA (2019) Acute kidney injury. Lancet (Lond Engl). 394(10212):1949–1964. https://doi.org/10.1016/S0140-6736(19)32563-2CrossRef

11.

Kellum JA et al (2017) Recovery after acute kidney injury. Am J Respir Crit Care Med 195(6):784–791. https://doi.org/10.1164/rccm.201604-0799OCCrossRefPubMedPubMedCentral

12.

Shah S et al (2020) Mortality and recovery associated with kidney failure due to acute kidney injury. Clin J Am Soc Nephrol CJASN. https://doi.org/10.2215/CJN.11200919CrossRefPubMed

13.

Yan P et al (2021) Acute kidney disease in hospitalized acute kidney injury patients. PeerJ 9:e11400. https://doi.org/10.7717/peerj.11400CrossRefPubMedPubMedCentral

14.

Venkatachalam MA et al (2015) Failed tubule recovery, AKI-CKD transition, and kidney disease progression. J Am Soc Nephrol 26(8):1765–1776. https://doi.org/10.1681/ASN.2015010006CrossRefPubMedPubMedCentral

15.

Basile DP et al (2016) Progression after AKI: understanding maladaptive repair processes to predict and identify therapeutic treatments. J Am Soc Nephrol JASN 27(3):687–697. https://doi.org/10.1681/ASN.2015030309CrossRefPubMed

16.

Bomsztyk K, Denisenko O (2013) Epigenetic alterations in acute kidney injury. Semin Nephrol 33(4):327–340. https://doi.org/10.1016/j.semnephrol.2013.05.005CrossRefPubMedPubMedCentral

17.

Docherty M-H et al (2019) Cellular senescence in the kidney. J Am Soc Nephrol JASN 30(5):726–736. https://doi.org/10.1681/ASN.2018121251CrossRefPubMed

18.

Ferenbach DA, Bonventre JV (2015) Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD. Nat Rev Nephrol 11(5):264–276. https://doi.org/10.1038/nrneph.2015.3CrossRefPubMedPubMedCentral

19.

Tang C et al (2021) Mitochondrial quality control in kidney injury and repair. Nat Rev Nephrol 17(5):299–318. https://doi.org/10.1038/s41581-020-00369-0CrossRefPubMed

20.

Singh AP et al (2020) Molecular connectivity of mitochondrial gene expression and OXPHOS biogenesis. Molecular Cell. https://doi.org/10.1016/j.molcel.2020.07.024CrossRefPubMedPubMedCentral

21.

Ratliff BB et al (2016) Oxidant mechanisms in renal injury and disease. Antioxid Redox Signal 25(3):119–146. https://doi.org/10.1089/ars.2016.6665CrossRefPubMedPubMedCentral

22.

Coppolino G et al (2018) Oxidative stress and kidney function: a brief update. Curr Pharmaceut Design 24(40):4794–4799. https://doi.org/10.2174/1381612825666190112165206CrossRef

23.

Mapuskar KA et al (2019) Persistent increase in mitochondrial superoxide mediates cisplatin-induced chronic kidney disease. Redox Biol. https://doi.org/10.1016/j.redox.2018.09.020CrossRefPubMed

24.

Kim J et al (2009) Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice. Am J Physiol Ren Physiol 297(2):F461–F470. https://doi.org/10.1152/ajprenal.90735.2008CrossRef

25.

Szeto HH (2014) First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. Br J Pharmacol 171(8):2029–2050. https://doi.org/10.1111/bph.12461CrossRefPubMedPubMedCentral

26.

Zhang X, Agborbesong E, Li X (2021) The role of mitochondria in acute kidney injury and chronic kidney disease and its therapeutic potential. Int J Mol Sci. https://doi.org/10.3390/ijms222011253CrossRefPubMedPubMedCentral

27.

Ding W et al (2016) Mitochondrial reactive oxygen species-mediated NLRP3 inflammasome activation contributes to aldosterone-induced renal tubular cells injury. Oncotarget 7(14):17479–17491. https://doi.org/10.18632/oncotarget.8243CrossRefPubMedPubMedCentral

28.

Popov L-D (2020) Mitochondrial biogenesis: an update. J Cell Mol Med 24(9):4892–4899. https://doi.org/10.1111/jcmm.15194CrossRefPubMedPubMedCentral

29.

Jamwal S, Blackburn JK, Elsworth JD (2021) PPARγ/PGC1α signaling as a potential therapeutic target for mitochondrial biogenesis in neurodegenerative disorders. Pharmacol Thera 219:107705. https://doi.org/10.1016/j.pharmthera.2020.107705CrossRef

30.

Chambers JM, Wingert RA (2020) PGC-1α in disease: recent renal insights into a versatile metabolic regulator. Cells. https://doi.org/10.3390/cells9102234CrossRefPubMedPubMedCentral

31.

Tran M et al (2011) PGC-1α promotes recovery after acute kidney injury during systemic inflammation in mice. J Clin Invest 121(10):4003–4014. https://doi.org/10.1172/JCI58662CrossRefPubMedPubMedCentral

32.

Portilla D et al (2002) Alterations of PPARalpha and its coactivator PGC-1 in cisplatin-induced acute renal failure. Kidney Int 62(4):1208–1218CrossRefPubMed

33.

Cherry AD et al (2014) Peroxisome proliferator-activated receptor γ co-activator 1-α as a critical co-activator of the murine hepatic oxidative stress response and mitochondrial biogenesis in Staphylococcus aureus sepsis. J Biol Chem 289(1):41–52. https://doi.org/10.1074/jbc.M113.512483CrossRefPubMed

34.

Fontecha-Barriuso M et al (2020) The role of PGC-1α and mitochondrial biogenesis in kidney diseases. Biomolecules. https://doi.org/10.3390/biom10020347CrossRefPubMedPubMedCentral

35.

Kelly DP, Scarpulla RC (2004) Transcriptional regulatory circuits controlling mitochondrial biogenesis and function. Genes Dev 18(4):357–368CrossRefPubMed

36.

Yuan Y et al (2012) Activation of peroxisome proliferator-activated receptor-γ coactivator 1α ameliorates mitochondrial dysfunction and protects podocytes from aldosterone-induced injury. Kidney Int. 82(7):771–789. https://doi.org/10.1038/ki.2012.188CrossRefPubMed

37.

Platt C, Coward RJ (2017) Peroxisome proliferator activating receptor-γ and the podocyte. Nephrol Dial Transp 32(3):423–433. https://doi.org/10.1093/ndt/gfw320CrossRef

38.

Collier JB, Schnellmann RG (2020) Extracellular signal-regulated kinase 1/2 regulates NAD metabolism during acute kidney injury through microRNA-34a-mediated NAMPT expression. Cell Mol Life Sci CMLS. 77(18):3643–3655. https://doi.org/10.1007/s00018-019-03391-zCrossRefPubMed

39.

Gibbs WS et al (2018) 5-HT receptor regulates mitochondrial homeostasis and its loss potentiates acute kidney injury and impairs renal recovery. Am J Physiol Ren Physiol 315(4):F1119–F1128. https://doi.org/10.1152/ajprenal.00077.2018CrossRef

40.

Fernandez-Marcos PJ, Auwerx J (2011) Regulation of PGC-1α, a nodal regulator of mitochondrial biogenesis. Am J Clin Nutr 93(4):884S – 8890. https://doi.org/10.3945/ajcn.110.001917CrossRefPubMedPubMedCentral

41.

Stallons LJ, Whitaker RM, Schnellmann RG (2014) Suppressed mitochondrial biogenesis in folic acid-induced acute kidney injury and early fibrosis. Toxicol Lett 224(3):326–332. https://doi.org/10.1016/j.toxlet.2013.11.014CrossRefPubMed

42.

Jiang M et al (2019) Combined blockade of Smad3 and JNK pathways ameliorates progressive fibrosis in folic acid nephropathy. Front Pharmacol. 10:880. https://doi.org/10.3389/fphar.2019.00880CrossRefPubMedPubMedCentral

43.

Chan DC (2020) Mitochondrial dynamics and its involvement in disease. Annu Rev Pathol 15:235–259. https://doi.org/10.1146/annurev-pathmechdis-012419-032711CrossRefPubMed

44.

Zhan M et al (2013) Mitochondrial dynamics: regulatory mechanisms and emerging role in renal pathophysiology. Kidney Int 83(4):568–581. https://doi.org/10.1038/ki.2012.441CrossRefPubMedPubMedCentral

45.

Tilokani L et al (2018) Mitochondrial dynamics: overview of molecular mechanisms. Essays Biochem 62(3):341–360. https://doi.org/10.1042/EBC20170104CrossRefPubMedPubMedCentral

46.

Tang C et al (2018) PINK1-PRKN/PARK2 pathway of mitophagy is activated to protect against renal ischemia-reperfusion injury. Autophagy. 14(5):880–897. https://doi.org/10.1080/15548627.2017.1405880CrossRefPubMedPubMedCentral

47.

Lei R et al (2018) Mitophagy plays a protective role in iodinated contrast-induced acute renal tubular epithelial cells injury. Cell Physiol Biochem Int J Exp Cell Physiol Biochem Pharmacol 46(3):975–985. https://doi.org/10.1159/000488827CrossRef

48.

Wang Y et al (2020) Mitophagy in acute kidney injury and kidney repair. Cells. https://doi.org/10.3390/cells9020338CrossRefPubMedPubMedCentral

49.

Yan Y et al (2020) miR-214 represses mitofusin-2 to promote renal tubular apoptosis in ischemic acute kidney injury. Am J Physiol Ren Physiol 318(4):F878–F887. https://doi.org/10.1152/ajprenal.00567.2019CrossRef

50.

Wang Y et al (2020) Drp1-mediated mitochondrial fission promotes renal fibroblast activation and fibrogenesis. Cell Death Dis 11(1):29. https://doi.org/10.1038/s41419-019-2218-5CrossRefPubMedPubMedCentral

51.

Gall JM et al (2015) Conditional knockout of proximal tubule mitofusin 2 accelerates recovery and improves survival after renal ischemia. J Am Soc Nephrol JASN. 26(5):1092–1102. https://doi.org/10.1681/ASN.2014010126CrossRefPubMed

52.

Livingston MJ et al (2019) Clearance of damaged mitochondria via mitophagy is important to the protective effect of ischemic preconditioning in kidneys. Autophagy 15(12):2142–2162. https://doi.org/10.1080/15548627.2019.1615822CrossRefPubMedPubMedCentral

53.

Lin Q et al (2019) PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation. Redox Biol. 26:101254. https://doi.org/10.1016/j.redox.2019.101254CrossRefPubMedPubMedCentral

54.

Inoue T, Maekawa H, Inagi R (2019) Organelle crosstalk in the kidney. Kidney Int 95(6):1318–1325. https://doi.org/10.1016/j.kint.2018.11.035CrossRefPubMed

55.

Senft D, Ronai ZEA (2015) UPR, autophagy, and mitochondria crosstalk underlies the ER stress response. Trends Biochem Sci. 40(3):141–148. https://doi.org/10.1016/j.tibs.2015.01.002CrossRefPubMedPubMedCentral

56.

Lombardi AA, Elrod JW (2017) Mediating ER-mitochondrial cross-talk. Science (New York NY). 358(6363):591–592. https://doi.org/10.1126/science.aaq0141CrossRef

57.

Maekawa H, Inagi R (2019) Pathophysiological role of organelle stress/crosstalk in AKI-to-CKD. Trans Semin Nephrol 39(6):581–588. https://doi.org/10.1016/j.semnephrol.2019.10.007CrossRef

58.

Kezic A et al (2016) Mitochondria-targeted antioxidants: future perspectives in kidney ischemia reperfusion injury. Oxid Med Cell Long 2016:2950503. https://doi.org/10.1155/2016/2950503CrossRef

59.

Dare AJ et al (2015) Protection against renal ischemia-reperfusion injury in vivo by the mitochondria targeted antioxidant. MitoQ Redox Biol 5:163–168. https://doi.org/10.1016/j.redox.2015.04.008CrossRefPubMed

60.

Song J et al (2022) Mitochondrial targeted antioxidant SKQ1 ameliorates acute kidney injury by inhibiting ferroptosis. Oxid Med Cell Longev 2022:1–19. https://doi.org/10.1155/2022/2223957CrossRef

61.

Plotnikov EY et al (2011) Mechanisms of nephroprotective effect of mitochondria-targeted antioxidants under rhabdomyolysis and ischemia/reperfusion. Biochimica et Biophysica Acta 1812(1):77–86. https://doi.org/10.1016/j.bbadis.2010.09.008CrossRefPubMed

62.

Mukhopadhyay P et al (2012) Mitochondrial-targeted antioxidants represent a promising approach for prevention of cisplatin-induced nephropathy. Free Radical Biol Med 52(2):497–506. https://doi.org/10.1016/j.freeradbiomed.2011.11.001CrossRef

63.

Birk AV et al (2013) The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. J Am Soc Nephrol JASN. 24(8):1250–1261. https://doi.org/10.1681/ASN.2012121216CrossRefPubMed

64.

Szeto HH et al (2017) Mitochondria protection after acute ischemia prevents prolonged upregulation of IL-1 and IL-18 and arrests CKD. J Am Soc Nephrol JASN. 28(5):1437–1449. https://doi.org/10.1681/ASN.2016070761CrossRefPubMed

65.

Liu S et al (2014) Novel cardiolipin therapeutic protects endothelial mitochondria during renal ischemia and mitigates microvascular rarefaction, inflammation, and fibrosis. Am J Physiol Ren Physiol 306(9):F970–F980. https://doi.org/10.1152/ajprenal.00697.2013CrossRef

66.

Szeto HH et al (2015) Improving mitochondrial bioenergetics under ischemic conditions increases warm ischemia tolerance in the kidney. Am J Physiol Ren Physiol 308(1):F11–F21. https://doi.org/10.1152/ajprenal.00366.2014CrossRef

67.

Tran MT et al (2016) PGC1α drives NAD biosynthesis linking oxidative metabolism to renal protection. Nature. 531(7595):528–532. https://doi.org/10.1038/nature17184CrossRefPubMedPubMedCentral

68.

Lempiäinen J et al (2012) AMPK activator AICAR ameliorates ischaemia reperfusion injury in the rat kidney. Br J Pharmacol 166(6):1905–1915. https://doi.org/10.1111/j.1476-5381.2012.01895.xCrossRefPubMedPubMedCentral

69.

Shin YJ et al (2015) Protective effects of quercetin against HgCl₂-induced nephrotoxicity in sprague-dawley rats. J Med Food. 18(5):524–534. https://doi.org/10.1089/jmf.2014.3242CrossRefPubMed

70.

Kitada M, Koya D (2013) Renal protective effects of resveratrol. Oxidat Med Cell Long. 2013:568093. https://doi.org/10.1155/2013/568093CrossRef

71.

Funk JA, Schnellmann RG (2013) Accelerated recovery of renal mitochondrial and tubule homeostasis with SIRT1/PGC-1α activation following ischemia-reperfusion injury. Toxicol Appl Pharmacol. 273(2):345–354. https://doi.org/10.1016/j.taap.2013.09.026CrossRefPubMedPubMedCentral

72.

Jesinkey SR et al (2014) Formoterol restores mitochondrial and renal function after ischemia-reperfusion injury. J Am Soc Nephrol JASN 25(6):1157–1162. https://doi.org/10.1681/ASN.2013090952CrossRefPubMed

73.

Cameron RB et al (2019) Proximal tubule -adrenergic receptor mediates formoterol-induced recovery of mitochondrial and renal function after ischemia-reperfusion injury. J Pharmacol Exp Thera 369(1):173–180. https://doi.org/10.1124/jpet.118.252833CrossRef

74.

Garrett SM et al (2014) Agonism of the 5-hydroxytryptamine 1F receptor promotes mitochondrial biogenesis and recovery from acute kidney injury. J Pharmacol Exp Thera 350(2):257–264. https://doi.org/10.1124/jpet.114.214700CrossRef

75.

Chen W et al (2018) Pioglitazone protects against renal ischemia-reperfusion injury via the AMP-activated protein kinase-regulated autophagy pathway. Front Pharmacol 9:851. https://doi.org/10.3389/fphar.2018.00851CrossRefPubMedPubMedCentral

76.

Suzuki T et al (2016) Mitochonic Acid 5 binds mitochondria and ameliorates renal tubular and cardiac myocyte damage. J Am Soc Nephrol JASN. 27(7):1925–1932. https://doi.org/10.1681/ASN.2015060623CrossRefPubMed

77.

Poyan Mehr A et al (2018) De novo NAD biosynthetic impairment in acute kidney injury in humans. Nat Med 24(9):1351–1359. https://doi.org/10.1038/s41591-018-0138-zCrossRefPubMed

78.

Katsyuba E et al (2018) De novo NAD synthesis enhances mitochondrial function and improves health. Nature 563(7731):354–359. https://doi.org/10.1038/s41586-018-0645-6CrossRefPubMedPubMedCentral

79.

Bouchez S et al (2018) Levosimendan in acute and advanced heart failure: an expert perspective on posology and therapeutic application. Cardiovasc Drugs Therapy 32(6):617–624. https://doi.org/10.1007/s10557-018-6838-2CrossRef

80.

Cassidy-Stone A et al (2008) Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization. Dev Cell 14(2):193–204. https://doi.org/10.1016/j.devcel.2007.11.019CrossRefPubMedPubMedCentral

81.

Brooks C et al (2009) Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models. J Clin Investig 119(5):1275–1285. https://doi.org/10.1172/JCI37829CrossRefPubMedPubMedCentral

82.

Rosdah AA et al (2016) Mitochondrial fission—a drug target for cytoprotection or cytodestruction? Pharmacol Res Perspect. 4(3):e00235. https://doi.org/10.1002/prp2.235CrossRefPubMedPubMedCentral

83.

Tang W-X et al (2013) Amelioration of rhabdomyolysis-induced renal mitochondrial injury and apoptosis through suppression of Drp-1 translocation. J Nephrol. 26(6):1073–1082. https://doi.org/10.5301/jn.5000268CrossRefPubMed

84.

Perry HM et al (2018) Dynamin-related protein 1 deficiency promotes recovery from AKI. J Am Soc Nephrol JASN. 29(1):194–206. https://doi.org/10.1681/ASN.2017060659CrossRefPubMed

85.

Bordt EA et al (2017) The putative Drp1 inhibitor mdivi-1 is a reversible mitochondrial complex i inhibitor that modulates reactive oxygen species. Dev Cell. https://doi.org/10.1016/j.devcel.2017.02.020CrossRefPubMedPubMedCentral

86.

Cui J et al (2015) Rapamycin protects against gentamicin-induced acute kidney injury via autophagy in mini-pig models. Sci Rep 5:11256. https://doi.org/10.1038/srep11256CrossRefPubMedPubMedCentral

87.

Livingston MJ et al (2016) Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction. Autophagy 12(6):976–998. https://doi.org/10.1080/15548627.2016.1166317CrossRefPubMedPubMedCentral

88.

Zou D et al (2019) Oral delivery of nanoparticle urolithin A normalizes cellular stress and improves survival in mouse model of cisplatin-induced AKI American journal of physiology. Ren Physiol 317(5):F1255–F1264. https://doi.org/10.1152/ajprenal.00346.2019CrossRef

89.

Wang Z et al (2013) Redox-sensitive glycogen synthase kinase 3β-directed control of mitochondrial permeability transition: rheostatic regulation of acute kidney injury. Free Radical Biol Med 65:849–858. https://doi.org/10.1016/j.freeradbiomed.2013.08.169CrossRef

90.

Wang Z et al (2015) Pharmacological targeting of GSK3β confers protection against podocytopathy and proteinuria by desensitizing mitochondrial permeability transition. Br J Pharmacol. 172(3):895–909. https://doi.org/10.1111/bph.12952CrossRefPubMed

91.

Zhao K et al (2004) Cell-permeable peptide antioxidants targeted to inner mitochondrial membrane inhibit mitochondrial swelling, oxidative cell death, and reperfusion injury. J Biol Chem 279(33):34682–34690CrossRefPubMed

92.

Zhang W et al (2018) Rotenone ameliorates chronic renal injury caused by acute ischemia/reperfusion. Oncotarget 9(36):24199–24208. https://doi.org/10.18632/oncotarget.24733CrossRefPubMedPubMedCentral

93.

Aparicio-Trejo OE et al (2017) Curcumin prevents mitochondrial dynamics disturbances in early 5/6 nephrectomy: relation to oxidative stress and mitochondrial bioenergetics. BioFactors (Oxf, Engl) 43(2):293–310. https://doi.org/10.1002/biof.1338CrossRef

Titel: Mitochondrial quality control in acute kidney disease
verfasst von: Jingyi Sheng
Xian Li
Juan Lei
WeiHua Gan
Jiayu Song
Publikationsdatum: 17.02.2023
Verlag: Springer International Publishing
Erschienen in: Journal of Nephrology / Ausgabe 5/2023
Print ISSN: 1121-8428
Elektronische ISSN: 1724-6059
DOI: https://doi.org/10.1007/s40620-023-01582-3

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

„Jeder Fall von plötzlichem Tod muss obduziert werden!“

17.05.2024 Plötzlicher Herztod Nachrichten

Ein signifikanter Anteil der Fälle von plötzlichem Herztod ist genetisch bedingt. Um ihre Verwandten vor diesem Schicksal zu bewahren, sollten jüngere Personen, die plötzlich unerwartet versterben, ausnahmslos einer Autopsie unterzogen werden.

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

17.05.2024 Direkte orale Antikoagulanzien Nachrichten

Kommt es zu einer nichttraumatischen Hirnblutung, spielt es keine große Rolle, ob die Betroffenen zuvor direkt wirksame orale Antikoagulanzien oder Marcumar bekommen haben: Die Prognose ist ähnlich schlecht.

Schlechtere Vorhofflimmern-Prognose bei kleinem linken Ventrikel

17.05.2024 Vorhofflimmern Nachrichten

Nicht nur ein vergrößerter, sondern auch ein kleiner linker Ventrikel ist bei Vorhofflimmern mit einer erhöhten Komplikationsrate assoziiert. Der Zusammenhang besteht nach Daten aus China unabhängig von anderen Risikofaktoren.

Semaglutid bei Herzinsuffizienz: Wie erklärt sich die Wirksamkeit?

17.05.2024 Herzinsuffizienz Nachrichten

Bei adipösen Patienten mit Herzinsuffizienz des HFpEF-Phänotyps ist Semaglutid von symptomatischem Nutzen. Resultiert dieser Benefit allein aus der Gewichtsreduktion oder auch aus spezifischen Effekten auf die Herzinsuffizienz-Pathogenese? Eine neue Analyse gibt Aufschluss.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Die Highlights vom Kongress des American College of Cardiology 2024

Springer Medizin

Abstract

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 5/2023

Steroid resistant nephrotic syndrome with collapsing focal segmental glomerulosclerosis in a 12-year-old Japanese female after SARS-CoV-2 vaccination

Associations of health literacy with self-management behaviours and health outcomes in chronic kidney disease: a systematic review

Risk factors for development of acute kidney injury and acute kidney disease in critically ill children

Two cases of severe vitamin D3 intoxication treated with therapeutic plasma exchange and high cut-off hemodialysis

Chronic kidney disease, female infertility, and medically assisted reproduction: a best practice position statement by the Kidney and Pregnancy Group of the Italian Society of Nephrology